Morphological and functional differences in haemostatic axis between kidney transplanted and end‐stage renal disease patients
Summary End‐stage renal disease (ESRD) is characterized by several atherothrombotic abnormalities, and kidney transplant seems to improve most of them. However, because it is not clear which mechanism is responsible for such improvement, our purpose was to clarify that point.We conducted a cross sec...
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| Veröffentlicht in: | Transplant international 2005-09, Vol.18 (9), p.1036-1047 |
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| creator | Fiorina, Paolo Folli, Franco Ferrero, Elisabetta Orsenigo, Elena Finzi, Giovanna Mazzolari, Gabriella Placidi, Claudia Perego, Lucia Rosa, Stefano La Melandri, Marco Monti, Lucilla Capella, Carlo D'Angelo, Armando Staudacher, Carlo Secchi, Antonio |
| description | Summary
End‐stage renal disease (ESRD) is characterized by several atherothrombotic abnormalities, and kidney transplant seems to improve most of them. However, because it is not clear which mechanism is responsible for such improvement, our purpose was to clarify that point.We conducted a cross sectional study involving 30 ESRD patients, 30 ESRD kidney‐transplanted patients (Ktx) and 30 healthy controls (C) to evaluate platelet morphology and function, atherothrombotic profile, endothelial abnormalities and cytokine levels involved in the insulin resistance/endothelial dysfunction. (i) Platelet morphology: The ESRD group showed platelet size similar to the other two groups (ESRD = 3518 × 103 ± 549 × 103 nm2, C = 3075 × 103 ± 197 × 103 nm2, Ktx = 2862 × 103 ± 205 × 103 nm2) with similar platelet granules and number. (ii) Platelet surface glycoprotein: The CD41 and P‐Selectin were similar between groups. (iii) Platelet intracellular calcium: Resting intracellular calcium was statistically higher in ESRD compared to the C group (ESRD = 182.1 ± 34.5, Ktx = 126.7 ± 14.1, C = 72.0 ± 11.0 nM, P |
| doi_str_mv | 10.1111/j.1432-2277.2005.00173.x |
| format | Article |
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End‐stage renal disease (ESRD) is characterized by several atherothrombotic abnormalities, and kidney transplant seems to improve most of them. However, because it is not clear which mechanism is responsible for such improvement, our purpose was to clarify that point.We conducted a cross sectional study involving 30 ESRD patients, 30 ESRD kidney‐transplanted patients (Ktx) and 30 healthy controls (C) to evaluate platelet morphology and function, atherothrombotic profile, endothelial abnormalities and cytokine levels involved in the insulin resistance/endothelial dysfunction. (i) Platelet morphology: The ESRD group showed platelet size similar to the other two groups (ESRD = 3518 × 103 ± 549 × 103 nm2, C = 3075 × 103 ± 197 × 103 nm2, Ktx = 2862 × 103 ± 205 × 103 nm2) with similar platelet granules and number. (ii) Platelet surface glycoprotein: The CD41 and P‐Selectin were similar between groups. (iii) Platelet intracellular calcium: Resting intracellular calcium was statistically higher in ESRD compared to the C group (ESRD = 182.1 ± 34.5, Ktx = 126.7 ± 14.1, C = 72.0 ± 11.0 nM, P < 0.01). (iv) Hypercoagulability markers and natural anticoagulants: The Ktx and ESRD groups showed higher levels of hypercoagulability markers compared to the C group. A reduction in antithrombin activity was evident in ESRD compared to the Ktx group (P = 0.03). (v) Endothelial morphology: The ESRD group showed a thickened vessel basal membrane compared to the Ktx and C groups with more endothelial sufference. (vi) Insulin resistance and pro‐inflammatory cytokine profile: The ESRD showed a higher homeostasis model assessment provided equations for estimating insulin resistance (HOMA‐IR) compared to the Ktx and C groups (ESRD = 2.6 ± 0.3, Ktx = 1.8 ± 0.2, C =1.1 ± 0.1, P = 0.005) and increased soluble tumor neurosis factor α (sTNFα) (P < 0.05) and soluble vascular cell adhesion molecule (sVCAM) levels (P < 0.01). Positive correlations were evident among HOMA‐IR and sTNFα (P < 0.001) and sVCAM (P = 0.01), respectively. In a small subgroup of ESRD who underwent Ktx (five pts), our findings were confirmed at 1 year of follow‐up, suggesting an improvement of almost haemostatic abnormalities. Kidney transplant is associated with a better atherothrombotic profile in ESRD, platelet intracellular calcium and cytokines seem to be most influenced by the transplant, while most morphological abnormalities are retained.</description><identifier>ISSN: 0934-0874</identifier><identifier>EISSN: 1432-2277</identifier><identifier>DOI: 10.1111/j.1432-2277.2005.00173.x</identifier><identifier>PMID: 16101724</identifier><language>eng</language><publisher>Oxford, UK: Munksgaard International Publishers</publisher><subject>Adult ; Biological and medical sciences ; Blood Platelets - pathology ; Blood Platelets - ultrastructure ; Calcium - blood ; Cross-Sectional Studies ; Endothelium, Vascular - pathology ; end‐stage renal disease ; General aspects ; haemostasis ; Hemostasis ; Humans ; Insulin Resistance ; Interleukin-18 - blood ; Kidney Failure, Chronic - blood ; Kidney Failure, Chronic - pathology ; Kidney Failure, Chronic - physiopathology ; Kidney Failure, Chronic - surgery ; kidney transplant ; Kidney Transplantation ; Medical sciences ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Pharmacology. Drug treatments ; platelets ; Renal failure</subject><ispartof>Transplant international, 2005-09, Vol.18 (9), p.1036-1047</ispartof><rights>2006 INIST-CNRS</rights><rights>Copyright Blackwell Publishing Ltd. Sep 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4233-d5ecc5ce7e041f3f306bb59a53aa4b617de23a0455c78017ed4fdbf0ef8882b73</citedby><cites>FETCH-LOGICAL-c4233-d5ecc5ce7e041f3f306bb59a53aa4b617de23a0455c78017ed4fdbf0ef8882b73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1432-2277.2005.00173.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1432-2277.2005.00173.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27928,27929,45578,45579</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17350080$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16101724$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fiorina, Paolo</creatorcontrib><creatorcontrib>Folli, Franco</creatorcontrib><creatorcontrib>Ferrero, Elisabetta</creatorcontrib><creatorcontrib>Orsenigo, Elena</creatorcontrib><creatorcontrib>Finzi, Giovanna</creatorcontrib><creatorcontrib>Mazzolari, Gabriella</creatorcontrib><creatorcontrib>Placidi, Claudia</creatorcontrib><creatorcontrib>Perego, Lucia</creatorcontrib><creatorcontrib>Rosa, Stefano La</creatorcontrib><creatorcontrib>Melandri, Marco</creatorcontrib><creatorcontrib>Monti, Lucilla</creatorcontrib><creatorcontrib>Capella, Carlo</creatorcontrib><creatorcontrib>D'Angelo, Armando</creatorcontrib><creatorcontrib>Staudacher, Carlo</creatorcontrib><creatorcontrib>Secchi, Antonio</creatorcontrib><title>Morphological and functional differences in haemostatic axis between kidney transplanted and end‐stage renal disease patients</title><title>Transplant international</title><addtitle>Transpl Int</addtitle><description>Summary
End‐stage renal disease (ESRD) is characterized by several atherothrombotic abnormalities, and kidney transplant seems to improve most of them. However, because it is not clear which mechanism is responsible for such improvement, our purpose was to clarify that point.We conducted a cross sectional study involving 30 ESRD patients, 30 ESRD kidney‐transplanted patients (Ktx) and 30 healthy controls (C) to evaluate platelet morphology and function, atherothrombotic profile, endothelial abnormalities and cytokine levels involved in the insulin resistance/endothelial dysfunction. (i) Platelet morphology: The ESRD group showed platelet size similar to the other two groups (ESRD = 3518 × 103 ± 549 × 103 nm2, C = 3075 × 103 ± 197 × 103 nm2, Ktx = 2862 × 103 ± 205 × 103 nm2) with similar platelet granules and number. (ii) Platelet surface glycoprotein: The CD41 and P‐Selectin were similar between groups. (iii) Platelet intracellular calcium: Resting intracellular calcium was statistically higher in ESRD compared to the C group (ESRD = 182.1 ± 34.5, Ktx = 126.7 ± 14.1, C = 72.0 ± 11.0 nM, P < 0.01). (iv) Hypercoagulability markers and natural anticoagulants: The Ktx and ESRD groups showed higher levels of hypercoagulability markers compared to the C group. A reduction in antithrombin activity was evident in ESRD compared to the Ktx group (P = 0.03). (v) Endothelial morphology: The ESRD group showed a thickened vessel basal membrane compared to the Ktx and C groups with more endothelial sufference. (vi) Insulin resistance and pro‐inflammatory cytokine profile: The ESRD showed a higher homeostasis model assessment provided equations for estimating insulin resistance (HOMA‐IR) compared to the Ktx and C groups (ESRD = 2.6 ± 0.3, Ktx = 1.8 ± 0.2, C =1.1 ± 0.1, P = 0.005) and increased soluble tumor neurosis factor α (sTNFα) (P < 0.05) and soluble vascular cell adhesion molecule (sVCAM) levels (P < 0.01). Positive correlations were evident among HOMA‐IR and sTNFα (P < 0.001) and sVCAM (P = 0.01), respectively. In a small subgroup of ESRD who underwent Ktx (five pts), our findings were confirmed at 1 year of follow‐up, suggesting an improvement of almost haemostatic abnormalities. Kidney transplant is associated with a better atherothrombotic profile in ESRD, platelet intracellular calcium and cytokines seem to be most influenced by the transplant, while most morphological abnormalities are retained.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Blood Platelets - pathology</subject><subject>Blood Platelets - ultrastructure</subject><subject>Calcium - blood</subject><subject>Cross-Sectional Studies</subject><subject>Endothelium, Vascular - pathology</subject><subject>end‐stage renal disease</subject><subject>General aspects</subject><subject>haemostasis</subject><subject>Hemostasis</subject><subject>Humans</subject><subject>Insulin Resistance</subject><subject>Interleukin-18 - blood</subject><subject>Kidney Failure, Chronic - blood</subject><subject>Kidney Failure, Chronic - pathology</subject><subject>Kidney Failure, Chronic - physiopathology</subject><subject>Kidney Failure, Chronic - surgery</subject><subject>kidney transplant</subject><subject>Kidney Transplantation</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Pharmacology. Drug treatments</subject><subject>platelets</subject><subject>Renal failure</subject><issn>0934-0874</issn><issn>1432-2277</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcuKFDEYhYMoTjv6ChIE3VWZaycNbmTwMjAiyLgOqeTPTNrqVJlUMd0rfQSf0ScxfcEBVwZCEvKdw0kOQpiSltbxet1SwVnDmFItI0S2hFDF2-0DtPh78RAtyIqLhmglztCTUtaEEKYleYzO6JJWARML9OPTkMfboR9uorM9tsnjMCc3xSHVo48hQIbkoOCY8K2FzVAmO0WH7TYW3MF0B5Dwt-gT7PCUbSpjb9ME_mAFyf_--asqbgBXm4NjAVsAj9UE0lSeokfB9gWendZz9PX9u-uLj83V5w-XF2-vGicY542X4Jx0oIAIGnjgZNl1cmUlt1Z0S6o8MG6JkNIpXZ8GXgTfBQJBa806xc_Rq6PvmIfvM5TJbGJx0NewMMzFLLXQdfIKvvgHXA9zrtGLYXQl1UppWiF9hFweSskQzJjjxuadocTsGzJrsy_C7Isw-4bMoSGzrdLnJ_-524C_F54qqcDLE2BLrSTUP3Wx3HOKS0I0qdybI3cXe9j9dwBz_eWybvgfo96vWQ</recordid><startdate>200509</startdate><enddate>200509</enddate><creator>Fiorina, Paolo</creator><creator>Folli, Franco</creator><creator>Ferrero, Elisabetta</creator><creator>Orsenigo, Elena</creator><creator>Finzi, Giovanna</creator><creator>Mazzolari, Gabriella</creator><creator>Placidi, Claudia</creator><creator>Perego, Lucia</creator><creator>Rosa, Stefano La</creator><creator>Melandri, Marco</creator><creator>Monti, Lucilla</creator><creator>Capella, Carlo</creator><creator>D'Angelo, Armando</creator><creator>Staudacher, Carlo</creator><creator>Secchi, Antonio</creator><general>Munksgaard International Publishers</general><general>Blackwell Publishing</general><general>Blackwell Publishing Ltd</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>200509</creationdate><title>Morphological and functional differences in haemostatic axis between kidney transplanted and end‐stage renal disease patients</title><author>Fiorina, Paolo ; Folli, Franco ; Ferrero, Elisabetta ; Orsenigo, Elena ; Finzi, Giovanna ; Mazzolari, Gabriella ; Placidi, Claudia ; Perego, Lucia ; Rosa, Stefano La ; Melandri, Marco ; Monti, Lucilla ; Capella, Carlo ; D'Angelo, Armando ; Staudacher, Carlo ; Secchi, Antonio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4233-d5ecc5ce7e041f3f306bb59a53aa4b617de23a0455c78017ed4fdbf0ef8882b73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Blood Platelets - pathology</topic><topic>Blood Platelets - ultrastructure</topic><topic>Calcium - blood</topic><topic>Cross-Sectional Studies</topic><topic>Endothelium, Vascular - pathology</topic><topic>end‐stage renal disease</topic><topic>General aspects</topic><topic>haemostasis</topic><topic>Hemostasis</topic><topic>Humans</topic><topic>Insulin Resistance</topic><topic>Interleukin-18 - blood</topic><topic>Kidney Failure, Chronic - blood</topic><topic>Kidney Failure, Chronic - pathology</topic><topic>Kidney Failure, Chronic - physiopathology</topic><topic>Kidney Failure, Chronic - surgery</topic><topic>kidney transplant</topic><topic>Kidney Transplantation</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Pharmacology. Drug treatments</topic><topic>platelets</topic><topic>Renal failure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fiorina, Paolo</creatorcontrib><creatorcontrib>Folli, Franco</creatorcontrib><creatorcontrib>Ferrero, Elisabetta</creatorcontrib><creatorcontrib>Orsenigo, Elena</creatorcontrib><creatorcontrib>Finzi, Giovanna</creatorcontrib><creatorcontrib>Mazzolari, Gabriella</creatorcontrib><creatorcontrib>Placidi, Claudia</creatorcontrib><creatorcontrib>Perego, Lucia</creatorcontrib><creatorcontrib>Rosa, Stefano La</creatorcontrib><creatorcontrib>Melandri, Marco</creatorcontrib><creatorcontrib>Monti, Lucilla</creatorcontrib><creatorcontrib>Capella, Carlo</creatorcontrib><creatorcontrib>D'Angelo, Armando</creatorcontrib><creatorcontrib>Staudacher, Carlo</creatorcontrib><creatorcontrib>Secchi, Antonio</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Transplant international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fiorina, Paolo</au><au>Folli, Franco</au><au>Ferrero, Elisabetta</au><au>Orsenigo, Elena</au><au>Finzi, Giovanna</au><au>Mazzolari, Gabriella</au><au>Placidi, Claudia</au><au>Perego, Lucia</au><au>Rosa, Stefano La</au><au>Melandri, Marco</au><au>Monti, Lucilla</au><au>Capella, Carlo</au><au>D'Angelo, Armando</au><au>Staudacher, Carlo</au><au>Secchi, Antonio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Morphological and functional differences in haemostatic axis between kidney transplanted and end‐stage renal disease patients</atitle><jtitle>Transplant international</jtitle><addtitle>Transpl Int</addtitle><date>2005-09</date><risdate>2005</risdate><volume>18</volume><issue>9</issue><spage>1036</spage><epage>1047</epage><pages>1036-1047</pages><issn>0934-0874</issn><eissn>1432-2277</eissn><abstract>Summary
End‐stage renal disease (ESRD) is characterized by several atherothrombotic abnormalities, and kidney transplant seems to improve most of them. However, because it is not clear which mechanism is responsible for such improvement, our purpose was to clarify that point.We conducted a cross sectional study involving 30 ESRD patients, 30 ESRD kidney‐transplanted patients (Ktx) and 30 healthy controls (C) to evaluate platelet morphology and function, atherothrombotic profile, endothelial abnormalities and cytokine levels involved in the insulin resistance/endothelial dysfunction. (i) Platelet morphology: The ESRD group showed platelet size similar to the other two groups (ESRD = 3518 × 103 ± 549 × 103 nm2, C = 3075 × 103 ± 197 × 103 nm2, Ktx = 2862 × 103 ± 205 × 103 nm2) with similar platelet granules and number. (ii) Platelet surface glycoprotein: The CD41 and P‐Selectin were similar between groups. (iii) Platelet intracellular calcium: Resting intracellular calcium was statistically higher in ESRD compared to the C group (ESRD = 182.1 ± 34.5, Ktx = 126.7 ± 14.1, C = 72.0 ± 11.0 nM, P < 0.01). (iv) Hypercoagulability markers and natural anticoagulants: The Ktx and ESRD groups showed higher levels of hypercoagulability markers compared to the C group. A reduction in antithrombin activity was evident in ESRD compared to the Ktx group (P = 0.03). (v) Endothelial morphology: The ESRD group showed a thickened vessel basal membrane compared to the Ktx and C groups with more endothelial sufference. (vi) Insulin resistance and pro‐inflammatory cytokine profile: The ESRD showed a higher homeostasis model assessment provided equations for estimating insulin resistance (HOMA‐IR) compared to the Ktx and C groups (ESRD = 2.6 ± 0.3, Ktx = 1.8 ± 0.2, C =1.1 ± 0.1, P = 0.005) and increased soluble tumor neurosis factor α (sTNFα) (P < 0.05) and soluble vascular cell adhesion molecule (sVCAM) levels (P < 0.01). Positive correlations were evident among HOMA‐IR and sTNFα (P < 0.001) and sVCAM (P = 0.01), respectively. In a small subgroup of ESRD who underwent Ktx (five pts), our findings were confirmed at 1 year of follow‐up, suggesting an improvement of almost haemostatic abnormalities. Kidney transplant is associated with a better atherothrombotic profile in ESRD, platelet intracellular calcium and cytokines seem to be most influenced by the transplant, while most morphological abnormalities are retained.</abstract><cop>Oxford, UK</cop><pub>Munksgaard International Publishers</pub><pmid>16101724</pmid><doi>10.1111/j.1432-2277.2005.00173.x</doi><tpages>12</tpages></addata></record> |
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| ispartof | Transplant international, 2005-09, Vol.18 (9), p.1036-1047 |
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| source | MEDLINE; Access via Wiley Online Library; EZB-FREE-00999 freely available EZB journals |
| subjects | Adult Biological and medical sciences Blood Platelets - pathology Blood Platelets - ultrastructure Calcium - blood Cross-Sectional Studies Endothelium, Vascular - pathology end‐stage renal disease General aspects haemostasis Hemostasis Humans Insulin Resistance Interleukin-18 - blood Kidney Failure, Chronic - blood Kidney Failure, Chronic - pathology Kidney Failure, Chronic - physiopathology Kidney Failure, Chronic - surgery kidney transplant Kidney Transplantation Medical sciences Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Pharmacology. Drug treatments platelets Renal failure |
| title | Morphological and functional differences in haemostatic axis between kidney transplanted and end‐stage renal disease patients |
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